By using immunohistochemistry LSAB method and imaging analysis technique, the expression of α1-antitrypsinase (α1-AT) in 41 cases of bronchioalveolar carcinoma (BAC) was quantitatively detected to explore the relationship between αl-AT expression in BAC tissues and clinical pathology. The results showed that the total positive rate for αl-AT expression was 85.4%. The positive rate for αl-AT expression in alveolar BAC was 100%, with the immunity reactive staining intensity being significantly higher than in papillary BAC, mucinous BAC or sclerosing BAC (P＜0.05). The positive rate in papillary BAC was 93.3%, with the intensity higher mucinous BAC or sclerosing BAC (P＜0.01); The positive rate in both mucinous BAC and sclerosing BAC was 66.7% (P＞0.05); The expression intensity in lymph node metastatic group was obviously lower than that in the group without metastasis (P＜0.01); The patients with mucinous BAC were diagnosed at a younger age than those with other histologic types of BAC (P＜0.05). It was suggested that BAC cells could also produce αl-AT. Detection of α1-AT could be used as a new method to diagnose BAC and might play a role in assessing BAC metastasis.

By using immunohistochemistry LSAB method and imaging analysis technique, the expression of α1-antitrypsinase (α1-AT) in 41 cases of bronchioalveolar carcinoma (BAC) was quantitatively detected to explore the relationship between αl-AT expression in BAC tissues and clinical pathology. The results showed that the total positive rate for αl-AT expression was 85.4%. The positive rate for αl-AT expression in alveolar BAC was 100%, with the immunity reactive staining intensity being significantly higher than in papillary BAC, mucinous BAC or sclerosing BAC (P＜0.05). The positive rate in papillary BAC was 93.3%, with the intensity higher mucinous BAC or sclerosing BAC (P＜0.01); The positive rate in both mucinous BAC and sclerosing BAC was 66.7% (P＞0.05); The expression intensity in lymph node metastatic group was obviously lower than that in the group without metastasis (P＜0.01); The patients with mucinous BAC were diagnosed at a younger age than those with other histologic types of BAC (P＜0.05). It was suggested that BAC cells could also produce αl-AT. Detection of α1-AT could be used as a new method to diagnose BAC and might play a role in assessing BAC metastasis.

Sesamin, a lipid-soluble lignin originally isolated from sesame seeds, which induces cancer cell apoptosis and autophagy. In the present study, has been reported that sesamin induces apoptosis via several pathways in human lung cancer cells. However, whether mitophagy is involved in sesamin induced lung cancer cell apotosis remains unclear. This study, the anticancer activity of sesamin in lung cancer was studied by reactive oxygen species (ROS) and mitophagy. A549 cells were treated with sesamin, and cell viability, migration ability, and cell cycle were assessed using the CCK8 assay, scratch-wound test, and flow cytometry, respectively. ROS levels, mitochondrial membrane potential, and apoptosis were examined by flow cytometric detection of DCFH-DA fluorescence and by using JC-1 and TUNEL assays. The results indicated that sesamin treatment inhibited the cell viability and migration ability of A549 cells and induced G0/G1 phase arrest. Furthermore, sesamin induced an increase in ROS levels, a reduction in mitochondrial membrane potential, and apoptosis accompanied by an increase in cleaved caspase-3 and cleaved caspase-9. Additionally, sesamin triggered mitophagy and increased the expression of PINK1 and translocation of Parkin from the cytoplasm to the mitochondria. However, the antioxidant N-acetyl-L-cysteine clearly reduced the oxidative stress and mitophagy induced by sesamin. Furthermore, we found that cyclosporine A (an inhibitor of mitophagy) decreased the inhibitory effect of sesamin on A549 cell viability. Collectively, our data indicate that sesamin exerts lethal effects on lung cancer cells through the induction of ROS-mediated mitophagy and mitochondrial apoptosis.

Sesamin, a lipid-soluble lignin originally isolated from sesame seeds, which induces cancer cell apoptosis and autophagy. In the present study, has been reported that sesamin induces apoptosis via several pathways in human lung cancer cells. However, whether mitophagy is involved in sesamin induced lung cancer cell apotosis remains unclear. This study, the anticancer activity of sesamin in lung cancer was studied by reactive oxygen species (ROS) and mitophagy. A549 cells were treated with sesamin, and cell viability, migration ability, and cell cycle were assessed using the CCK8 assay, scratch-wound test, and flow cytometry, respectively. ROS levels, mitochondrial membrane potential, and apoptosis were examined by flow cytometric detection of DCFH-DA fluorescence and by using JC-1 and TUNEL assays. The results indicated that sesamin treatment inhibited the cell viability and migration ability of A549 cells and induced G0/G1 phase arrest. Furthermore, sesamin induced an increase in ROS levels, a reduction in mitochondrial membrane potential, and apoptosis accompanied by an increase in cleaved caspase-3 and cleaved caspase-9. Additionally, sesamin triggered mitophagy and increased the expression of PINK1 and translocation of Parkin from the cytoplasm to the mitochondria. However, the antioxidant N-acetyl-L-cysteine clearly reduced the oxidative stress and mitophagy induced by sesamin. Furthermore, we found that cyclosporine A (an inhibitor of mitophagy) decreased the inhibitory effect of sesamin on A549 cell viability. Collectively, our data indicate that sesamin exerts lethal effects on lung cancer cells through the induction of ROS-mediated mitophagy and mitochondrial apoptosis.